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Cardiopulmonary Exam 1 > Upper Respiratory Diseases of Horses > Flashcards

Upper Respiratory Diseases of Horses Flashcards

1
Q

Etiology of Strangles

A

Streptococcus equi equi

highly host adapted

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2
Q

Epizootiology of Strangles

A

Transmission:

  • direct contact
  • indirect: contaminated buckets, feed, pasture…

Outbreaks occur where large groups of animals are brought together

  • morbidity: 30-100%
  • mortality: <10%
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3
Q

Pathogenesis of Strangles

A

ingestion or inhalation –> attachment to tonsils and translocation below mucosa in the lymphatics –> multiplication in local lymph nodes –> lymph node abscessation –> dissemination may occur (hematogenous or via lymphatics)

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4
Q

Clinical signs of Strangles

A
  • incubation period 3-14 days
  • fever, depression
  • bilateral nasal discharge (serous then purulent)
  • lymphadenopathy (submandibular and retropharyngeal)
  • respiratory distress
  • abscesses may occur anywhere on the body
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5
Q

Chronic carriers of Strangles

A
  • most horses stop shedding 3-6 weeks after resolution of clinical signs
  • some horses will become chronic asymptomatic carriers
    • guttural pouch is the site of carriage in >80% of horses
    • shedding may last for several months, even years
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6
Q

Diagnosis of Strangles

A
  • abscessed lymph nodes are sufficient for a presumptive dx
  • culture or PCR amplification
    • abscess aspirate
    • nasal or pharyngeal swab
    • nasal flush (3x negative)***
    • guttural pouch flush (1x negative)
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7
Q

Treatment of Strangles

A
  • early (before abscessation): +/- penicillin
  • horses with lymph node abscessation
    • promote maturation and drainage of abscessed lymph nodes
    • no abx unless pneumonia or respiratory distress
    • supportive therapy
  • horses exposed to S. equi equi: penicillin
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8
Q

Strangles Complications

A
  • pneumonia
  • guttural pouch empyema and/or chondroids
  • bastard strangles (metastatic)
  • myocarditis, endocarditis (rare)
  • glomerulonephritis
  • purpura hemorrhagica
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9
Q

purpura hemorrhagica (strangles)

A
  • acute necrotizing immune-mediated vasculitis
  • 2-4 weeks after outbreak
  • pathophysiology:
    • immune complexes -> deposition in blood vessels -> complement activation and mediator release -> vessel wall necrosis
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10
Q

Purpura hemorrhagica clinical signs

A
  • warm and painful edema of the limb, ventral abdomen and face
    • may progress to skin necrosis and sloughing
  • petechial hemorrhage
  • +/- fever
  • stiffness, reluctance to move
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11
Q

Diagnosis of purpura hemorrhagica

A
  • history and clinical signs
  • skin biopsy
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12
Q

Treatment of purpura hemorrhagica

A
  • systemic antimicrobials
    • penicillin +/- gram-negative coverage
  • corticosteroids
  • supportive therapy (NSAIDs, hydrotherapy, bandages)
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13
Q

Vaccination for Strangles

A
  • intramuscular
    • M protein extracts
  • intranasal (Pinnacle IN)
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14
Q

Guttural pouch anatomy

A
  • diverticulum of the Eustachian tubes
    • medial compartment:
      • internal carotid
      • cranial nerves IX, X, XI, XII
      • cranial cervical ganglion
    • lateral compartment
      • external carotid artery
      • maxillary artery
      • cranial nerve VII
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15
Q

Guttural pouch empyema

A

accumulation of exudate in the guttural pouches

  • unilateral or bilateral
  • sometimes the exudate may solidify (chondroids)
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16
Q

Clinical signs of guttural pouch empyema

A
  • nasal discharge when head down (greater on the affected side)
  • rarely dysphagia
  • not usually malodorous
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17
Q

Diagnosis of GP empyema

A
  • endoscopy
  • radiographs: fluid line or chondroids
  • culture:
    • Streptococcus equi zooepidemicus
    • Streptococcus equi equi
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18
Q

Treatment of GP empyema

A
  • lavage with large volumes of saline
  • antibiotics
  • sx to remove chondroids
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19
Q

Guttural pouch mycosis

A

fungal infections often over a major blood vessel (usually internal carotid)

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20
Q

Clinical signs of GP mycosis

A
  • epistaxis
  • dysphagia
  • other (Horner’s syndrome, laryngeal hemiplegia…)
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21
Q

Diagnosis of GP mycosis

A
  • endoscopy
  • culture
    • Emericella nidulans
    • Aspergillus spp. or other fungi
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22
Q

Treatment of GP mycosis

A
  • surgical: proximal and distal occlusion of the affected artery
  • medical: not recommended if severe epistaxis
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23
Q

Guttural pouch tympany

A
  • distension of one or both guttural pouches with air (horses less than 1 year of age)
  • clinical signs:
    • external swelling in parotid area
    • dyspnea if severe
    • rarely dysphagia
  • diagnosis:
    • clinical signs
  • treatment:
    • surgical
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24
Q

Sinusitis

A
  • primary
    • maxillary sinus is most commonly affected
    • S. equi zooepidemicus is commonly involved
  • secondary
    • tooth root abscess
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25
Q

Clinical signs of sinusitis

A
  • nasal discharge (unilateral)
  • ozena (halitosis)
  • ocular discharge
  • facial sensitivity/deformity
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26
Q

Diagnosis of sinusitis

A
  • percussion
  • radiographs
  • endoscopy
  • oral exam
  • CT
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27
Q

Treatment of sinusitis

A
  • primary
    • systemic antibiotics
    • sinus flush
  • secondary
    • systemic antibiotics
    • tooth extraction
    • tooth repulsion through a maxillary sinus flap
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28
Q

Viral respiratory diseases

A
  • influenza
  • Herpes virus (rhinopneumonitis)
  • clinical signs: fever, cough, and nasal discharge
  • diagnosis:
    • virus isolation
    • ***PCR amplification
    • serology
    • antigen detection
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29
Q

Equine Influenza

A
  • most common cause of severe epidemics of upper respiratory disease in horses
  • orthomyxovirus with a RNA genome
  • only influenza type A affects horses
  • antigenic determinants
    • hemagglutinin (HA)
    • neuraminidase (NA)
30
Q

Pathogenesis of Equine Influenza

A
  • only two types have been recognized in horses
    • A/equine 1 (H7N7)
    • A/equine 2 (H3N8) major subtype in horses
    • antigenic drift
  • incubation 1-3 days
  • infect mainly 1-3 year old horses in training
  • infection -> adhesion to respiratory epithelium -> desquamation of ciliated cells -> decreased mucociliary clearance
  • low mortality, high morbidity (up to 100%)
31
Q

Clinical signs of Equine Influenza

A
  • acute onset of fever, anorexia and depression
  • dry cough
  • serous nasal discharge
  • submandibular lymph nodes may be slightly enlarged
32
Q

Diagnosis of Equine Influenza

A
  • viral isolation: influenza is difficult to isolate
  • RT-PCR amplification
  • serology: retrospective dx only
  • Influenza A Antigen Detection Kit (rapid)
33
Q

Complications of Equine Influenza

A
  • bacterial pneumonia/pleuropneumonia
  • myositis, myocarditis
34
Q

Treatment of Equine Influenza

A
  • rest: at least three weeks
  • NSAIDs to control fever
  • antibiotics if secondary bacterial pneumonia develop
  • specific antiviral therapy is usually not warranted
35
Q

Equine Influenza Immunity and Vax

A
  • Immunity: protection lasts 1 year following natural infection
  • vax (killed IM): transient systemic IgG response, every 6 months
  • vaccination (MLV IN): protects for 6-12 months
  • Canary Pox Vector Vaccine: useful in foals of vaccinated dams
36
Q

Equine Herpesvirus

A

EHV-1: abortion, perinatal dz and death, neurological form (EHM), respiratory dz

EHV-2: immunosuppression?, keratoconjunctivitis

EHV-3: equine coital exanthema

EHV-4: respiratory disease (rhinopneumonitis)

EHV-5: EMPF

37
Q

EHV 1 & EHV 4 Pathogenesis

A
  • most common in young horses (0-3 years)
  • responsible for 15-20% of outbreaks of URT dz
  • up to 85% of horses carry EHV-1 and/or EHV-4 in a latent state (lymph nodes, trigeminal ganglia)
  • acquisition by inhalation or recrudescence of a latent infection
  • incubation period 2-10 days
  • viremia is common is EHV-1 infections
38
Q

Diagnosis of EHV-1 & 4

A
  • virus isolation or qPCR amplification
    • nasal swabs
    • whole blood (EHV-1)
  • serology
39
Q

Vaccination of EHV-1 & 4

A
  • currently available vaccines
    • EHV-1, EHV-4 or both
    • inactivated or modified live
    • label claim: abortion vs respiratory dz
  • cross-protection between EHV-1 and EHV-4
40
Q

Foal Pneumonia

A
  • 1-10 months
  • leading cause of morbidity and mortality
  • inhalation of aerosolized or dust-borne pathogens
  • neonates
    • bacteremia
    • hematogenous spread of bacteria to lungs
41
Q

Clinical signs of Foal Pneumonia

A
  • cough
  • nasal discharge (bilateral)
  • fever
  • increased respiratory rate
  • respiratory distress

(any combination)

42
Q

Diagnosis of Foal Pneumonia

A
  • abnormal lung sounds
  • hematology
  • radiology and u/s
  • tracheobronchial aspiration (cytology, gram stain, culture)
  • response to tx
43
Q

Etiologic agents of Foal Pneumonia

A
  • Streptococcus equi zooepidemicus
    • most commonly isolated
  • Rhodococcus equi
  • other bacteria may be primary or occur in association with S. zooepidemicus or R. equi
    • ​**Pasteurella, E. coli…
44
Q

Treatment of Foal Pneumonia

A
  • Abx
  • oxygen therapy
  • duration of therapy based on: resolution of clinical signs, normal WBC count and fibrinogen concentrations, diagnostic imaging
  • minimum of 10 days
45
Q

Prognosis of Foal Pneumonia

A

most cases make a complete recovery if diagnosed early and treated appropriatedly

46
Q

Pathogenesis of Rhodococcus equi Pneumonia

A
  • Gram-positive facultative intracellular pathogen
  • can survive and replicate in macrophages
  • normal inhabitant in soil
  • infection by inhalation
  • devastating disease on some farms
47
Q

Clinical manifestations of R. equi Pneumonia

A
  • 1 to 6 months of age
  • bronchopneumonia
  • intestinal manifestations
  • nonseptic immune-mediated polysynovitis
  • septic arthritis and osteomyelitis
  • other manifestations (uveitis, abbscesses)
48
Q

Diagnosis of R. equi Pneumonia

A
  • hematology
  • radiography and u/s
  • tracheobronchial aspiration: only way to make a definitive diagnosis
    • cytology, gram stain, culture, PCR
49
Q

Treatment of R. equi Pneumonia

A
  • macrolide and rifampin
    • penetrates caseous material
    • achieve good intracellular levels
  • long term therapy is require (4-9 weeks)
  • macrolides suppress sweating -> hyperthermia
50
Q

Prognosis of R. equi Pneumonia

A
  • survival rate 60-80%
  • affected foals are slightly less likely to race
51
Q

Prevention of R. equi Pneumonia

A
  • decreasing size of infective challenge
    • isolate affected foals
    • prevent grass destruction and dust formation
  • earlier recognition of the disease
  • hyperimmune plasma
    • decrease the incidence and severity of the disease
52
Q

Pneumonia

A

infection involving the lung and parenchyma

53
Q

pleuropneumonia

A

pneumonia or lung abscess that extends to and invovles the visceral pleura

54
Q

Causes of pleural effusion

A
  • pneumonia
  • pleuropneumonia
  • hemothorax
  • penetrating chest wound
  • neoplasia
  • hypoproteinemia
  • congestive heart failure
55
Q

pathophysiology of pneumonia/pleuropneumonia

A
  • viral infection, toxic gases, stress (transport, race), malnutrition, or general anesthesia
    • -> decreased number and bactericidal activity of alveolar macrophages ->
  • OR excessive number of virulent bacteria ->

= pneumonia/pleuropneumonia

56
Q

Clinical signs of pneumonia/pleuropneumonia

A
  • fever
  • anorexia, dperession
  • tachypnea, respiratory distress
  • cough
  • pain on palpation of the thorax
  • bilateral nasal discharge (hemorrhagic or purulent)
  • fetid breath
  • ventral edema
  • colic-like signs
  • weight loss in chronic cases
57
Q

Infectious agents of pneumonia/pleuropneumonia

A
  • S. equi zooepidemicus
  • Gram-negative bacteria (Pasteurella, E. coli…)
  • Anaerobes (Bacteroides, Eubacterium…)
58
Q

Diagnosis of pneumonia/pleuropneumonia

A
  • auscultation (absence of or decreased lung sounds ventrally)
  • percussion (horizontal line with resonant sounds dorsally and dull sounds ventrally)
  • pleurodynia (pleural pain)
  • hematology
  • u/s
  • radiography
  • tracheobronchial aspiration (cytology, culture)
  • thoracocentesis (cytology, culture)
59
Q

Treatment of pneumonia/pleuropneumonia

A
  • antibiotics
    • initial: broad-spectrum abx
    • ideal: based on C & S testing
    • long term therapy is often required (2-24 wks)
  • pleural drainage
  • supportive care
  • thoracotomy and rib resection (in chronic cases only)
60
Q

Complications of pneumonia/pleuropneumonia

A
  • endotoxemia and thrombophlebitis
  • laminitis
  • pleural and/or pulmonary abscess formation
  • pneumothorax
  • pericarditis (rare)
61
Q

Prognosis of pneumonia/pleuropneumonia

A

depends on severity and duration of clinical signs prior to therapy

62
Q

Exercise-Induced Pulmonary Hemorrhage (EIPH)

A
  • presence of blood in the airways after inense exercise
  • pulmonary hemorrhage (caudodorsal lung fields)
  • incidence
    • 5% of race horses will show epistaxis
    • up to 90% of race horses have EIPH
  • effects on performance-rule out other causes of exercise intolerance
63
Q

Diagnosis of EIPH

A
  • endoscopy
  • cytological examination (TBA or BAL)
    • hemosiderin-laden macrophages-Prussian blue stain
  • thoracic radiography
64
Q

Pathogenesis of EIPH

A
  • failure of pulmonary capillaries during exercise
  • pulmonary capillary pressure increased
65
Q

Treatment of EIPH

A
  • Furosemide (loop diuretic)
    • pre-race admin to horses with EIPH permitted by most states
    • does not prevent hemorrhage but decreases severity
  • nasal strips?
66
Q

Heaves

A
  • Equine asthma, RAO
  • mature horses (>3, often > 7 yo)
  • in northern US, stabled horses during winter
  • in southern US, more prevalent during summer on pasture
67
Q

Pathogenesis of Heaves

A

Fungi/Actinomycetes, molds, endotoxins, other allergens, genetic predisposition –>

  • non-specific inflammation
  • hypersensitivity
    • type I (IgE)
    • Type III (IgG or IgM)

= Inflammatory mediator release (cytokines, leukotrienes, histamine…)

  • -> bronchiolitis, neutrophilic airway infiltration, excess mucus, bronchoconstriction
68
Q

Clinical signs of Heaves

A

mild:

  • intermittent cough
  • exercise intolerance
  • abnormal lung sounds
  • mild increase in resp rate

severe:

  • respiratory distress
  • marked abdominal effort during expiration (heave line)
  • weight loss
  • fever is not present unless the disease is complicated by a secondary bacterial infection
69
Q

Diagnosis of Heaves

A
  • history and physical exam
    • increased expiratory effort
    • crackles and expiratory wheezes
    • lack of fever
    • normal WBC count and fibrinogen
  • bronchoalveolar lavage
  • response to bronchodilators
70
Q

Treatment of Heaves

A
  • environmental changes
    • reduce dust and allergen exposure (avoid hay or soak/steam it, move inside, change pasture)
  • corticosteroids (most effective therapy)
    • 2-4 weeks
    • inhaled vs systemic
  • bronchodilators
    • relieve obstruction caused by airway smooth muscle contraction
    • do not treat primary problem
    • systemic vs inhaled

Cardiopulmonary Exam 1 (10 decks)

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